ArticleProceedings of the National Academy of Sciences of the United States of America2019
Phosphorylated claudin-16 interacts with Trpv5 and regulates transcellular calcium transport in the kidney.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Energy-Dependent Phosphate and Acid Transport for Bone Formation and Resorption.Journal of cellular biochemistry · 2025Review
- Renal expression of calcium and phosphorus transporters: contrasting responses to dietary calcium and microbial phytase in broilers and growing pigs.The British journal of nutrition · 2024Article
- Vitamin DScientific reports · 2024Article
- The odyssey of the TR(i)P journey to the cellular membrane.Frontiers in cell and developmental biology · 2024Review
- 24-h Urinary Calcium Excretion and Renal Outcomes in Hospitalized Patients with and without Chronic Kidney Disease.Journal of clinical medicine · 2023Article
- Pathophysiological aspects of the thick ascending limb and novel genetic defects: HELIX syndrome and transient antenatal Bartter syndrome.Pediatric nephrology (Berlin, Germany) · 2022Review
- Renal calcium and magnesium handling in Gitelman syndrome.American journal of translational research · 2022Review
- Differential localization patterns of claudin 10, 16, and 19 in human, mouse, and rat renal tubular epithelia.American journal of physiology. Renal physiology · 2021Article
- Structure, Function, and Regulation of the Blood-Brain Barrier Tight Junction in Central Nervous System Disorders.Frontiers in physiology · 2020Review
- Mouse Models of Human Claudin-Associated Disorders: Benefits and Limitations.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) was previously considered to be a paracellular channelopathy caused by mutations in the claudin-16 and claudin-19 genes. Here, we provide evidence that a missense FHHNC mutation c.908C>G (p.T303R) in the claudin-16 gene interferes with the phosphorylation in the claudin-16 protein. The claudin-16 protein carrying phosphorylation at residue T303 is localized in the distal convoluted tubule (DCT) but not in the thick ascending limb (TAL) of the mouse kidney. The phosphomimetic claudin-16 protein carrying the T303E mutation but not the wildtype claudin-16 or the T303R mutant protein increases the Trpv5 channel conductance and membrane abundance in human kidney cells. Phosphorylated claudin-16 and Trpv5 are colocalized in the luminal membrane of the mouse DCT tubule; phosphomimetic claudin-16 and Trpv5 interact in the yeast and mammalian cell membranes. Knockdown of claudin-16 gene expression in transgenic mouse kidney delocalizes Trpv5 from the luminal membrane in the DCT. Unlike wildtype claudin-16, phosphomimetic claudin-16 is delocalized from the tight junction but relocated to the apical membrane in renal epithelial cells because of diminished binding affinity to ZO-1. High-Ca
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